Mercury is a known neurotoxin; methylmercury is one of the most potent forms due to its ability to cross both the blood-brain and placental barriers. Unlike less toxic inorganic mercury, about 95% of dietary methylmercury is absorbed into the bloodstream, entering the hepatic portal circulation. The long, biological half-time of methylmercury (45-70 days) is attributed to extensive enterohepatic recycling, which is interrupted when methylmercury is demethylated by gut microbiota and excreted in feces. Thus gut microbial function is important to detoxification via its role in human metabolism and elimination of methylmercury. Conversely, evidence from human studies indicates not all methylmercury in the gut is demethylated, while inorganic Hg methylation by an archeon (isolated from human feces) is also possible. Inorganic mercury (or methylmercury) exposure induced changes in gut microbe communities; however data were limited to studies involving monkeys, crustaceans, and earthworms. Human studies are needed to establish bi-directional associations between gut microbiota, dietary methylmercury intake, and accumulation of methylmercury in tissues. To address this knowledge gap, we will leverage our prospective birth and child cohort study in China, to investigate associations between prenatal/postnatal methylmercury exposure and gut microbiota assessed in children's stools. The following includes the specific aims: Aim 1. Establish the impacts of prenatal and postnatal methylmercury exposure through rice ingestion on children's neurodevelopment, evaluated using the Bayley Scales of Infant Development. Aim 2. Assess the relative taxonomic abundance and diversity of gut microbiota (phylum, class, order, family, and genus levels) in children's stool samples using 16S rRNA gene profiling, to investigate associations between gut microbes, methylmercury exposure (prenatal/postnatal), and other confounders. Aim 3. Establish whether variability in methylmercury metabolism and exposure corresponds to microbial detoxification via mercury resistance genes (merA and merB) quantified in children's stool samples. Results from this study will clarify our understanding of the mechanisms by which gut microbes contribute to variability in children's methylmercury metabolism and exposure, potentially impacting offspring development.